Prostaglandin F(2α) inhibits acidification in H+-secreting epithelia

R. D. Page, Thomas Yorio

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

The role of prostaglandins in the regulation of acidification mechanisms in H+-secreting epithelia has been investigated in the abdominal skin of the southern leopard frog, Rana pipiens. Exogenous administration of prostaglandin (PG) E2 and PGF(1α) (10-7 M) to the serosal media of paired skins mounted in modified Ussing chambers showed no significant alteration on H+ excretion rates. PGF(2α) exhibited a dose-dependent inhibition of acidification in both the mucosal and serosal media of animals in normal acid-base states. The ED50 was determined to be 5 x 10-8 M. Animals placed in an NH4Cl-induced chronic metabolic acidosis demonstrated enhanced H+ excretion from normal which was inhibited by PGF(2α) (10-8 M). Frogs treated with ibuprofen (30 mg/kg/day for 3 days) stimulated mucosal acidification to a magnitude similar to the chronic metabolic acidosis animal, and this was inhibited by PGF(2α) (10-8 M) during the recovery phase. PGF(2α) produced effects on both the mucosal proton excretion system and the serosal Na+/H+ exchanger mechanism. PGF(2α) appears to function in this H+-secreting epithelia to maintain a low basal H+ excretion rate and to regulate intracellular pH.

Original languageEnglish
Pages (from-to)929-933
Number of pages5
JournalJournal of Pharmacology and Experimental Therapeutics
Volume252
Issue number3
StatePublished - 1 Jan 1990

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Prostaglandins F
Epithelium
Rana pipiens
Acidosis
Skin
Sodium-Hydrogen Antiporter
Ibuprofen
Dinoprostone
Anura
Prostaglandins
Protons
Acids

Cite this

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title = "Prostaglandin F(2α) inhibits acidification in H+-secreting epithelia",
abstract = "The role of prostaglandins in the regulation of acidification mechanisms in H+-secreting epithelia has been investigated in the abdominal skin of the southern leopard frog, Rana pipiens. Exogenous administration of prostaglandin (PG) E2 and PGF(1α) (10-7 M) to the serosal media of paired skins mounted in modified Ussing chambers showed no significant alteration on H+ excretion rates. PGF(2α) exhibited a dose-dependent inhibition of acidification in both the mucosal and serosal media of animals in normal acid-base states. The ED50 was determined to be 5 x 10-8 M. Animals placed in an NH4Cl-induced chronic metabolic acidosis demonstrated enhanced H+ excretion from normal which was inhibited by PGF(2α) (10-8 M). Frogs treated with ibuprofen (30 mg/kg/day for 3 days) stimulated mucosal acidification to a magnitude similar to the chronic metabolic acidosis animal, and this was inhibited by PGF(2α) (10-8 M) during the recovery phase. PGF(2α) produced effects on both the mucosal proton excretion system and the serosal Na+/H+ exchanger mechanism. PGF(2α) appears to function in this H+-secreting epithelia to maintain a low basal H+ excretion rate and to regulate intracellular pH.",
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Prostaglandin F(2α) inhibits acidification in H+-secreting epithelia. / Page, R. D.; Yorio, Thomas.

In: Journal of Pharmacology and Experimental Therapeutics, Vol. 252, No. 3, 01.01.1990, p. 929-933.

Research output: Contribution to journalArticle

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AB - The role of prostaglandins in the regulation of acidification mechanisms in H+-secreting epithelia has been investigated in the abdominal skin of the southern leopard frog, Rana pipiens. Exogenous administration of prostaglandin (PG) E2 and PGF(1α) (10-7 M) to the serosal media of paired skins mounted in modified Ussing chambers showed no significant alteration on H+ excretion rates. PGF(2α) exhibited a dose-dependent inhibition of acidification in both the mucosal and serosal media of animals in normal acid-base states. The ED50 was determined to be 5 x 10-8 M. Animals placed in an NH4Cl-induced chronic metabolic acidosis demonstrated enhanced H+ excretion from normal which was inhibited by PGF(2α) (10-8 M). Frogs treated with ibuprofen (30 mg/kg/day for 3 days) stimulated mucosal acidification to a magnitude similar to the chronic metabolic acidosis animal, and this was inhibited by PGF(2α) (10-8 M) during the recovery phase. PGF(2α) produced effects on both the mucosal proton excretion system and the serosal Na+/H+ exchanger mechanism. PGF(2α) appears to function in this H+-secreting epithelia to maintain a low basal H+ excretion rate and to regulate intracellular pH.

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